Heart failure is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles (particularly the left ventricle) to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues.
Heart failure has been classified by the New York Heart Association (NYHA) into four classes of progressively worsening symptoms and diminished exercise capacity. Class I corresponds to no limitation wherein ordinary physical activity does not cause undue fatigue, shortness of breath, or palpitation. Class II corresponds to slight limitation of physical activity wherein such patients are comfortable at rest, but wherein ordinary physical activity results in fatigue, shortness of breath, palpitations or angina. Class III corresponds to a marked limitation of physical activity wherein, although patients are comfortable at rest, even less than ordinary activity will lead to symptoms. Class IV corresponds to inability to carry on any physical activity without discomfort, wherein symptoms of heart failure are present even at rest and where increased discomfort is experienced with any physical activity.
The current standard treatment for heart failure is typically centered on medical treatment using angiotensin converting enzyme (ACE) inhibitors, diuretics, beta-blockade, and digitalis. Cardiac resynchronization therapy (CRT) may also be employed, if a bi-ventricular pacing device is implanted. Briefly, CRT seeks to normalize asynchronous cardiac electrical activation and resultant asynchronous contractions associated with CHF by delivering synchronized pacing stimulus to both ventricles. The stimulus is synchronized so as to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis, et al., entitled “Multi-Electrode Apparatus And Method For Treatment Of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer, et al., entitled “Apparatus And Method For Reversal Of Myocardial Remodeling With Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann, et al., entitled “Method And Apparatus For Maintaining Synchronized Pacing”.
Pulmonary edema is a swelling and/or fluid accumulation in the lungs often caused by heart failure (i.e. the edema represents one of the “congestives” of CHF.) Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs. This can cause severe respiratory problems and, left untreated, can be fatal. Pulmonary edema is usually associated with relatively severe forms of heart failure and is often asymptomatic until the edema itself becomes severe, i.e. the patient is unaware of the pulmonary edema until it has progressed to a near fatal state when respiration suddenly becomes quite difficult.
In view of the potential severity of heart failure/pulmonary edema, it is highly desirable to detect the onset of these conditions within a patient and to track the progression thereof so that appropriate therapy can be provided. Many patients suffering heart failure/pulmonary edema already have pacemakers or ICDs implanted therein or are candidates for such devices. Accordingly, it is desirable to provide such devices with the capability to automatically detect and track heart failure/pulmonary edema. Heretofore, a number of attempts have been made to provide for monitoring of physiological parameters associated with heart failure/pulmonary edema using implantable cardiac devices in conjunction with physiological sensors. In particular, it has been recognized that LV EDP often increases due to heart failure or pulmonary edema. (See, for example, discussions of Frank-Starling mechanisms in Braunwald et al., Heart Failure: A Textbook of Cardiovascular Medicine, 6th Ed., Ch. 16, pp. 503-533.) Accordingly, a pressure sensor may be mounted in the left ventricle for directly measuring blood pressure therein. A pacemaker, ICD or other implanted device then receives signals from the pressure sensor, from which it determines LV EDP. Heart failure/pulmonary edema may then be detected and tracked based on LV EDP. See, for example, U.S. Pat. No. 6,438,408 to Mulligan, et al., entitled “Implantable Medical Device For Monitoring Congestive Heart Failure”; U.S. Pat. No. 6,277,078 to Porat, et al., entitled “System and method for monitoring a parameter associated with the performance of a heart”; U.S. Pat. No. 6,666,826 to Salo, et al., entitled “Method and apparatus for measuring left ventricular pressure”; U.S. Pat. No. 6,580,946 to Struble, entitled “Pressure-modulated rate-responsive cardiac pacing”; and U.S. Patent Application 2002/0120200 of Brockway et al., entitled “Devices, Systems and Methods For Endocardial Pressure Measurement.”
Heretofore, however, such techniques have met with limited success. A significant problem with techniques for measuring LV EDP using a pressure sensor is that identifying the end diastolic phase of the pressure signal is non-trivial. Typically, pressure signals are generated by the pressure sensor more or less continuously and the implanted device must analyze the signals to identify the end diastolic phase of the heartbeat. This can consume considerable data processing resources within the device itself, which are preferably reserved for other device functions, such as controlling overdrive pacing, CRT pacing, atrial fibrillation (AF) suppression therapy, and the like. FIG. 1 illustrates an exemplary LV pressure profile 2 during a single heartbeat. The end of diastole is identified by vertical line 4. As can be seen, LV pressure increases sharply after the end of diastole. This is due to the closure of the mitral value and subsequent isovolumic contraction of the left ventricle, which increases blood pressure therein, prior to opening of the aortic valve. By continuously monitoring and storing LV pressure signals, the device can detect the sharp increase following closure of the mitral valve, then backtrack through the recorded data to read out the pressure value prior to the increase, i.e. the LV EDP value. This detection processes can consume considerable resources, both in terms of memory and processing time.
Accordingly, it would be highly desirable to provide improved techniques for detecting LV EDP using a pressure sensor, which do not consume significant data processing resources, and it is to that end that the invention is primarily directed. It is also desirable to provide techniques for detecting and tracking heart failure and/or pulmonary edema based on improved LV EDP measurements and other aspects of the invention are directed to that end as well.